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These data provide the first evidence for a physiologic role of these isoforms in RET pathway function.
Significantly, we show that introduction of mapk10 (show MAPK10 Proteins) mutations into ret heterozygotes enhanced the ENS deficit, supporting MAPK10 (show MAPK10 Proteins) as a Hirschsprung disease (HSCR (show EDNRB Proteins)) susceptibility locus. Our studies demonstrate that ret heterozygous zebrafish is a sensitized model, with many significant advantages over existing murine models, to explore the pathophysiology and complex genetics of HSCR (show EDNRB Proteins).
RET expression is investigated within the brain of zebrafish; both RET protein and mRNA are observed.
In animals lacking Ret or Gfra3 (show GFRA3 Proteins) function, myogenic gene expression is reduced in forming opercular muscles, but not in non-opercular muscles derived from the same muscle anlagen.
evaluation of noncoding sequences at the zebrafish ret locus conserved among teleosts, and at the human RET locus, conserved among mammals
genes beyond RET may be implicated in the genesis of sporadic cases of HD
BRAFV600E and RET/PTC and the expression of NF-kappaB (show NFKB1 Proteins) promote the proliferation and migration of papillary thyroid carcinoma cells in vitro.
The RET proto-oncogene located on chromosome 10q11.2 encodes a 1114-amino acid transmembrane receptor with a cadherin-related motif and a cysteine-rich domain in the extracellular domain.
We found 6 single nucleotide polymorphisms in RET that were independent contributors to Hischsprung disease
data establish differences in the mechanisms of RET9 and RET51 ubiquitylation and internalization that may influence the strength and duration of RET isoform signals and cellular outputs.
Study demonstrate that the kinesin and kinase domains of KIF5B (show KIF5B Proteins)-RET act together to establish an emergent microtubule and RAB (show HRB Proteins)-vesicle-dependent RET-SRC (show SRC Proteins)-EGFR (show EGFR Proteins)-FGFR (show FGFR2 Proteins) signaling hub. Study demonstrate that drugs designed to inhibit RET alone work poorly in KIF5B (show KIF5B Proteins)-RET-transformed cells.
RET knockdown significantly decreased xenografts tumor growth in vivo, confirming the oncogenic impact of RET signaling in vivo.
Each of these autosomal dominant syndromes results from a specific germline mutation in unique genes: MEN1 is due to pathogenic MEN1 variants (11q13), MEN2A and MEN2B are due to pathogenic RET variants (10q11.21), MEN4 (show CDKN1B Proteins) is due to pathogenic CDKN1B (show CDKN1B Proteins) variants (12p13.1), and the HPT-JT syndrome is due to pathogenic CDC73 (show CDC73 Proteins) variants (1q25).
RET p.C634F mutation is associated with Multiple Endocrine Neoplasia Type 2A with Cutaneous Lichen Amyloidosis.
These data support the inclusion of patients bearing RET alterations in ongoing and future molecularly enriched clinical trials to explore RXDX-105 efficacy across a variety of tumor types.
These results implicate EGFR (show EGFR Proteins) as a key regulator of RET activation in A+AD and suggest that EGFR (show EGFR Proteins) inhibitors may be therapeutic in patients with A+AD tumors even in the absence of an EGFR (show EGFR Proteins) or RET mutation.
p75 (show NGFR Proteins) is required for the development of the nonpeptidergic nociceptor lineage by fine-tuning Ret-mediated trophic support.
7-DHC efficiently supports Ret signaling in vitro.
Results showed that Mn-mediated age-related hearing loss involved a decreased expression and phosphorylation levels of c-Ret in spiral ganglion neurons.
Compromised Survival of Cerebellar Molecular Layer Interneurons Lacking GDNF Receptors GFRalpha1 (show GFRA1 Proteins) or RET Impairs Normal Cerebellar Motor Learning
Data show that NEDL2 regulates GDNF/Ret/Akt pathway depends on its Nedd8 ligase activity rather than ubiquitin ligase activity.
The cardiac GFRA2 (show GFRA2 Proteins) signaling pathway is distinct from the canonical pathway dependent on the RET tyrosine kinase (show TYRO3 Proteins).
Ret is essential to mediate GDNF's neuroprotective and neuroregenerative effect in a Parkinson disease mouse model.
Mechanistically, Ret is engaged in a positive feedback loop with Wnt/Wingless signalling, modulated by Src and Fak kinases.
Authors did not find evidence for genetic interaction between Ret and Sema3d (show SEMA3D Proteins) affecting survival, presence of myenteric plexus or intestine transcriptome.
findings uncover a novel spinal circuit that mediates crosstalk between touch and pain pathways and suggest that some early RET positive Dorsal Horn neurons could function as pain "gating" neurons.
This gene, a member of the cadherin superfamily, encodes one of the receptor tyrosine kinases, which are cell-surface molecules that transduce signals for cell growth and differentiation. This gene plays a crucial role in neural crest development, and it can undergo oncogenic activation in vivo and in vitro by cytogenetic rearrangement. Mutations in this gene are associated with the disorders multiple endocrine neoplasia, type IIA, multiple endocrine neoplasia, type IIB, Hirschsprung disease, and medullary thyroid carcinoma. Two transcript variants encoding different isoforms have been found for this gene. Additional transcript variants have been described but their biological validity has not been confirmed.
proto-oncogene tyrosine-protein kinase receptor Ret
, receptor tyrosine kinase
, ret proto-oncogene
, proto-oncogene tyrosine-protein kinase receptor Ret-like
, RET transforming sequence
, cadherin family member 12
, cadherin-related family member 16
, hydroxyaryl-protein kinase
, proto-oncogene c-Ret
, ret proto-oncogene (multiple endocrine neoplasia and medullary thyroid carcinoma 1, Hirschsprung disease)
, Ret gene for receptor tyrosin
, Ret proto-oncogene (multiple endocrine neoplasia MEN2A MEN2B and medullary thyroid carcinoma 1 Hirschsprung disease)
, ret tyrosine kinase